Further Observations on the Disruption of Rat Mesentery Mast Cells Caused by Compound 48/80, Antigen‐Antibody Reaction, Lecithinase A and Decylamine

Abstract

Högberg, B. and B. Uvnas. Further observations on the disruption of rat mesentery mast cells caused by compound 48/80, antigen‐antibody reaction, lecithinase A, and decylamine. The influence of pH, ionic milieu, temperature and enzyme inhibitors, on the disrupting action on rat mesentery mast cells of compound 48/80, antigen and decylamine has been investigated. A pH optimum around 7.4, the essentiality of Ca++ ions, the influence of temperature and the inhibitory action of various enzyme inhibitors, especially those blocking protein NH2‐groups and SH‐groups, supported the view that compound 48/80 and antigen disrupt the mast cells by activating a lytic enzyme attached to the mast cell membrane. Decylamine, on the other hand, is a surface active agent that disrupts mast cells by a non‐enzymatic mechanism.

PROCEEDINGS OF THE British Pharmacological Society

“…Maximal histamine release induced by A23187 was achieved between 33-39°C and the release declined above and below this temperature range. Essentially the same effect of temperature on anaphylactic histamine release from guinea pig lung and antigen induced mast cell disruption was reported by Schild (1957) andHogberg &Uvnas (1960).…”

“…We conclude that atropine in a low concentration blocks prejunctional muscarinic receptors; at higher concentrations it blocks in addition prejunctional aadrenoceptors. Anaphylactic histamine release from guinea pig lung and disruption of rat mast cell due to antigen is dependent on temperature (Mongar & Schild, 1957;Hogberg & Uvnas, 1960), and on oxidative or glycolytic metabolism (Parrot, 1942;Moussatche & Prouvost-Danon, 1962). The amount of histamine released by the antigen-antibody reaction in vitro was dependent on mast cell ATP content and during the release there was an increased utilization of ATP (Johansen & Chakravarty, 1975).…”

Parenteral Depot Method for Zinc Administration

“…Second, a cell regula tory role exists for zinc. For example, zinc antagonizes calcium in various cells [2][3][4][5][6][7][8]. We suggested that zinc might play a regula tory role in numerous cell types through in hibition of the function of the calcium-acti vated protein, calmodulin [9], Third, in addi tion to these fundamental roles, zinc has sev eral uses in clinical medicine, the first of which is the treatment o f zinc deficiency.…”

Proceedings of the Physiological Society

“…Furthermore, the observation that CN inhibition does not require pre-incubation of the tissue with CN suggests that this inhibition does not result from depletion of energy stores but rather from inactivation of enzymes other than cytochrome oxidase. Other workers have found that a nitrogen atmosphere did not inhibit antigen-induced rat mast-cell degranulation (Hogberg & Uvnas, 1960), and 5 mm CN was needed to inhibit this reaction (Mota, 1960). Thus, in the rat as in the guinea-pig the effect of CN might well be unrelated to inhibition of aerobic metabolism.…”